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| 1 | Expression, purification of a synthetic fuse-protein-TSF from PF4 and TSP1 fragments and its effect on angio-genesis and tumor growth显示文摘Sequences encoding PF4 (58-70) and TSP1 (429-459) were linked to yield a single gene TSF which encodes the fuse-protein of TSF. The gene was cloned into a pGEX-2T expression vector to generate a protein GST-TSF, which was strongly expressed in E. coli. The purified GST-TSF was degraded with thrombin to generate the protein TSF. With the methods of MTT and wound repair assay, the effects of TSF on the proliferation and migration of EC were detected, respectively. The results showed that TSF significantly suppressed BAEC proliferation and migration in a dose-dependent manner. The fuse protein GST-TSF, and the peptides PF4 (58-70) and TSP1 (429-459) also inhibited BAEC proliferation and migration, respectively, but their inhibition rates were not as high as TSF. Using the CAM assay, it was shown that TSF, GST-TSF, PF4 (58-70) and TSP1 (429-459) inhibited angiogenesis in chick CAM potentially, the effect of TSF was the highest. In vivo, the growth of Lewis lung carcinoma was potently inhibited by TSF | SHEN Xianrong JI Dongmei HU Youqing JIA Fuxing DENG Xinxian WANG Ling CHU Zhiyong JIANG Dingwen LEI Chengxiang HUANG Jiansheng HU Xinran REN Darning | 2001 | Chinese Science Bulletin2001，46，24： | 2 |
| 2 | SARS-CoV-2 immunity and functional recovery of COVID-19 patients 1-year after infection显示文摘The long-term immunity and functional recovery after SARS-CoV-2 infection have implications in preventive measures and patient quality of life.Here we analyzed a prospective cohort of 121 recovered COVID-19 patients from Xiangyang,China at 1-year after diagnosis.Among them,chemiluminescence immunoassay-based screening showed 99%(95%CI,98–100%)seroprevalence 10–12 months after infection,comparing to 0.8%(95%CI,0.7–0.9%)in the general population.Total anti-receptor-binding domain(RBD)antibodies remained stable since discharge,while anti-RBD IgG and neutralization levels decreased over time.A predictive model estimates 17%(95%CI,11–24%)and 87%(95%CI,80–92%)participants were still 50%protected against detectable and severe re-infection of WT SARS-CoV-2,respectively,while neutralization levels against B.1.1.7 and B.1.351 variants were significantly reduced.All non-severe patients showed normal chest CT and 21%reported COVID-19-related symptoms.In contrast,53%severe patients had abnormal chest CT,decreased pulmonary function or cardiac involvement and 79%were still symptomatic.Our findings suggest long-lasting immune protection after SARS-CoV-2 infection,while also highlight the risk of immune evasive variants and long-term consequences for COVID-19 survivors. | Yan Zhan Yufang Zhu Shanshan Wang Shijun Jia Yunling Gao Yingying Lu Caili Zhou Ran Liang Dingwen Sun Xiaobo Wang Zhibing Hou Qiaoqiao Hu Peng Du Hao Yu Chang Liu Miao Cui Gangling Tong Zhihua Zheng Yunsheng Xu Linyu Zhu Jin Cheng Feng Wu Yulan Zheng Peijun Liu Peng Hong | 2021 | Signal Transduction and Targeted Therapy2021，6，11： | 0 |
| 3 | SARS-CoV-2 N protein enhances the anti-apoptotic activity of MCL-1 to promote viral replication显示文摘Viral infection in respiratory tract usually leads to cell death,impairing respiratory function to cause severe disease.However,the diversity of clinical manifestations of SARS-CoV-2 infection increases the complexity and difficulty of viral infection prevention,and especially the high-frequency asymptomatic infection increases the risk of virus transmission.Studying how SARS-CoV-2 affects apoptotic pathway may help to understand the pathological process of its infection.Here,we uncovered SARS-CoV-2 imployed a distinct anti-apoptotic mechanism via its N protein.We found SARS-CoV-2 virus-like particles(trVLP)suppressed cell apoptosis,but the trVLP lacking N protein didn’t.Further study verified that N protein repressed cell apoptosis in cultured cells,human lung organoids and mice.Mechanistically,N protein specifically interacted with anti-apoptotic protein MCL-1,and recruited a deubiquitinating enzyme USP15 to remove the K63-linked ubiquitination of MCL-1,which stabilized this protein and promoted it to hijack Bak in mitochondria.Importantly,N protein promoted the replications of IAV,DENV and ZIKV,and exacerbated death of IAV-infected mice,all of which could be blocked by a MCL-1 specific inhibitor,S63845.Altogether,we identifed a distinct anti-apoptotic function of the N protein,through which it promoted viral replication.These may explain how SARS-CoV-2 effectively replicates in asymptomatic individuals without cuasing respiratory dysfunction,and indicate a risk of enhanced coinfection with other viruses.We anticipate that abrogating the N/MCL-1-dominated apoptosis repression is conducive to the treatments of SARS-CoV-2 infection as well as coinfections with other viruses. | Pan Pan Weiwei Ge Zhiwei Lei Wei luo Yuqing Liu Zhanwen Guan Lumiao Chen Zhenyang Yu Miaomiao Shen Dingwen Hu Qi Xiang Wenbiao Wang Pin Wan Mingfu Tian Yang Yu Zhen Luo Xulin Chen Heng Xiao Qiwei Zhang Xujing Liang Xin Chen Yongkui Li Jianguo Wu | 2023 | Signal Transduction and Targeted Therapy2023，8，6： | 0 |
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